Obesity is associated with increased levels of sympathetic nerve activity, which may lead to the development of hypertension. However, obesity does not always result in hypertension, and the increased levels of sympathetic activity in obese individuals do not correlate with the presence of hypertension. This strongly suggests that factors in addition to heightened sympathetic nerve activity are involved in the pathogenesis of hypertension in obesity. The long-term goal of this proposal is to explore the link between obesity and hypertension. Normally, insulin mediated vasodilation can offset increased sympathetic vasoconstriction. In this application, we test the hypothesis that the development of insulin-resistance exacerbates the hypertensive effects of increased sympathetic nerve activity in viscerally obese men. To test this hypothesis, the following specific aims will be addressed: Specific Aim 1: Compared to lean men, do viscerally obese men have higher levels of sympathetic nerve activity at rest and are the sympathetic nerve activity responses to sympathoexcitatory stimuli augmented? Specific Aim 2: In viscerally obese men, is the normal relation between sympathetic nerve activity and vascular resistance augmented to favor excessive vasoconstriction? Specific Aim 3: In viscerally obese men, is the normal blunting of sympathetic vasoconstriction by insulin attenuated in the face of insulin resistance?